Central and Peripheral Actions of Angiotensin II

The renin-angiotensin system is involved in fluid balance and cardiovascular function in several ways. Renin, the essential enzyme that converts angiotensinogen to angiotensin I, is released from the kidney to produce angiotensin under a variety of conditions, most notably low pressure in the renal artery. The increase of angiotensin I caused by renin leads to an increase of angiotensin II caused mostly by a conversion in the lungs through converting enzymes. Angiotensin II is a very powerful vasoconstrictor which acts directly on blood vessels to cause an increase in peripheral resistance and thereby increase blood pressure. At the same time, receptors in the adrenal gland are stimulated by angiotensin II to trigger the release of aldosterone. Aldosterone acts on the kidneys to retain sodium and by these two methods, vasoconstriction and aldosterone release, angiotensin II can effectively counteract low volume in the blood. So much has been known for many years and more recently, experiments with angiotensin II on the brain have shown two more effects that could be significant in counteracting decreased fluid volume in the body. When angiotensin II is injected into the brain ventricles, it produces thirst in rats and other species which compel the animals to drink and thereby, increase their fluid volume. At the same time, low doses of angiotensin directly injected into the brain cause release of vasopressin.